Down-Regulation of CEND1 Expression Contributes to The Progression and Temozolomide Resistance of Glioma

• 出版年: Cell Journal
• 主要な著者: Houjun Zhou, Bai Peng
• フォーマット: 論文
• 言語: 英語
• 出版事項: Royan Institute (ACECR), Tehran 2023-04-01
• 主題: cend1; glioma; proliferation; temozolomide
• オンライン･アクセス: https://www.celljournal.org/article_699793_4947675c2dfb8a990fa2b06e50c194ec.pdf

Objective: This study was conducted to clarify the expression characteristics of cell cycle exit and neuronal differentiation1 (CEND1) in glioma and its effects on the proliferation, migration, invasion, and resistance to temozolomide (TMZ) ofglioma cells.Materials and Methods: In this experimental study, CEND1 expression in glioma tissues and its relationship withpatients’ survival were analyzed through bioinformatics. Quantitative real-time polymerase chain reaction (qRT-PCR)and immunohistochemistry were performed to detect CEND1 expression in glioma tissues. The cell counting kit-8(CCK-8) method was adopted to detect cell viability and the effects of different concentrations of TMZ on the inhibitionrate of glioma cell proliferation, and the median inhibitory concentration of TMZ (IC50 value) was calculated. 5-Bromo-2'-deoxyuridine (BrdU), wound healing and Transwell assays were performed to evaluate the impacts of CEND1 onglioma cell proliferation, migration, and invasion. Besides, the Kyoto Encyclopedia of Genes and Genomes (KEGG)analysis, Gene Ontology (GO) analysis, and Gene Set Enrichment Analysis (GSEA) were applied to predict thepathways regulated by CEND1. Nuclear factor-kappa B p65 (NF-κB p65) and phospho-p65 (p-p65) expression weredetected by Western blot.Results: CEND1 expression was reduced in glioma tissues and cells, and its low expression was significantlyassociated with the shorter survival of glioma patients. CEND1 knockdown promoted glioma cell growth, migration,and invasion, and increased the IC50 value of TMZ, whereas up-regulating CEND1 expression worked oppositely.Genes co-expressed with CEND1 were enriched in the NF-κB pathway, and knocking down CEND1 facilitated p-p65expression, while CEND1 overexpression suppressed p-p65 expression.Conclusion: CEND1 inhibits glioma cell proliferation, migration, invasion, and resistance to TMZ by inhibiting the NF-κB pathway.